Cerebral Microhemorrhage

Viswanathan, Anand; Chabriat, Hugues

doi:10.1161/01.str.0000199847.96188.12

Cited by 270 publications

(192 citation statements)

References 58 publications

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“…Brain T2*-weighted MR imaging has been reported to demonstrate various etiologies of hypointense spots, which result from the deposition of hemosiderin (old hemorrhage), ferritin, calcium, the presence of other metallic materials and air [15]. It could also detect remnants of previous cerebral microbleeds (MBs) [16][17][18], which are usually defined as small, round, foci distinct from vascular flow voids, leptomeningeal hemosiderosis, and nonhemorrhagic subcortical mineralization [19]. MBs are considered as a general marker of microvascular vulnerability with the incidence of 3.1-6.4% [19,20] in healthy individuals, and 56% [21] in hypertensive patients.…”

Section: Discussionmentioning

confidence: 99%

“…It could also detect remnants of previous cerebral microbleeds (MBs) [16][17][18], which are usually defined as small, round, foci distinct from vascular flow voids, leptomeningeal hemosiderosis, and nonhemorrhagic subcortical mineralization [19]. MBs are considered as a general marker of microvascular vulnerability with the incidence of 3.1-6.4% [19,20] in healthy individuals, and 56% [21] in hypertensive patients. There are only two previous reports that refer to the relationship between T2*-weighted hypointense lesions and the presence of IE, and current study is the first case series discussing the clinical significance of the brain T2*-weighted MR imaging associated with IE [22][23][24].…”

Section: Discussionmentioning

confidence: 99%

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Significance of the T2*-weighted gradient echo brain imaging in patients with infective endocarditis

Morofuji

Morikawa

Tateishi

et al. 2010

Clinical Neurology and Neurosurgery

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Significance of the T2*-weighted gradient echo brain imaging in patients with infective endocarditis

Morofuji

Morikawa

Tateishi

et al. 2010

Clinical Neurology and Neurosurgery

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“…Deposits of hemosiderin are breakdown products of hemoglobin and reflect microhemorrages that occurred previously. 38 Immunohistological analysis revealed deposits of hemosiderin in Atm Ϫ/Ϫ retinas as early as 2 months of age, whereas WT retinas lacked evidence of such deposits ( Figure 5). …”

Section: Microhemorrhage Incidents In Atm ϫ/ϫ Micementioning

confidence: 99%

A Role for Vascular Deficiency in Retinal Pathology in a Mouse Model of Ataxia-Telangiectasia

Raz-Prag

Galron

Segev-Amzaleg

et al. 2011

The American Journal of Pathology

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Ataxia-telangiectasia is a multifaceted syndrome caused by null mutations in the ATM gene, which encodes the protein kinase ATM, a key participant in the DNA damage response. Retinal neurons are highly susceptible to DNA damage because they are terminally differentiated and have the highest metabolic activity in the central nervous system. In this study, we characterized the retina in young and aged Atmdeficient mice (Atm ؊/؊ ). At 2 months of age, angiography revealed faint retinal vasculature in Atm ؊/؊ animals relative to wild-type controls. This finding was accompanied by increased expression of vascular endothelial growth factor protein and mRNA. Fibrinogen, generally absent from wild-type retinal tissue, was evident in Atm ؊/؊ retinas, whereas mRNA of the tight junction protein occludin was significantly decreased. Immunohistochemistry labeling for occludin in 6-month-old mice showed that this decrease persists in advanced stages of the disease. Some brain disorders may have a vascular origin, 1,2 and vascular diseases can be directly linked to neuronal and synaptic dysfunction through changes in the blood flow, increase in blood-brain barrier permeability, and in nutrient supply. 3 A healthy brain relies on the proper function and communication of all cells comprising the neurovascular unit: neurons, astrocytes, brain endothelium, and vascular smooth muscle cells. 4 Impaired genomic stability interferes with cellular homeostasis and poses a constant threat to cellular viability. 5 The cell combats this threat by activating the DNA damage response (DDR), a complex signaling network that detects the DNA lesions, promotes their repair, and temporarily modulates cellular metabolism while the damage is being repaired. 6 The DDR is vigorously activated by DNA double-strand breaks (DSBs), a particularly cytotoxic DNA lesion induced by ionizing radiation, radiomimetic chemicals, and oxygen radicals. 7,8 The DNA damage response is a hierarchical process executed by sensor/mediator proteins that accumulate at DSB sites and by protein kinases that serve as transducers of the DNA damage alarm to numerous downstream effectors. 6 The primary transducer of the cellular response to DSBs is the protein kinase ATM, which phosphorylates many key players in the various branches of the DDR. 9 Ataxia-telangiectasia (A-T) is an autosomal recessive disorder caused by mutations in the ATM gene that encodes the ATM protein. 10 A-T is characterized by progressive neurodegeneration affecting mainly the cerebellum, which develops into severe neuromotor dysfunction;

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“…Akut semptomatik pontin mikrokanamalı bir olgu sunumu küçük damar hastalığı ve lökoaraiosis ve bunlarla ilişkili vasküler demans daha sık gözlenmektedir (5). Her ne kadar SMK tanımı perforan damarlarda kanama sonrası beyin dokusunda hasarlanma anlamı taşısa da parankimal kanama ve hasarlanma olmadan perivasküler mesafede hemosiderin birikimi olabileceği de düşünülmektedir (5).…”

Section: Gi̇ri̇ş Olguunclassified

Difusion weighted imaging characteristics differentiate acute symptomatic cerebral microbleeds from silent microbleeds: An acute pontine microhemorrhage case presentation

Yılmaz¹,

Topçuoğlu²,

Arsava³

2015

Türk Beyin Damar Hast Derg

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Cerebral Microhemorrhage

Cited by 270 publications

References 58 publications

Significance of the T2*-weighted gradient echo brain imaging in patients with infective endocarditis

Significance of the T2*-weighted gradient echo brain imaging in patients with infective endocarditis

A Role for Vascular Deficiency in Retinal Pathology in a Mouse Model of Ataxia-Telangiectasia

Difusion weighted imaging characteristics differentiate acute symptomatic cerebral microbleeds from silent microbleeds: An acute pontine microhemorrhage case presentation

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